Biochemical mutants affecting carbohydrate, pyrimidine and amino acid metabolism have been isolated from Chinese hamster cell lines (V79; CHO) in culture. Our purposes are to obtain information on genetic control of metabolism in mammalian cells and to elucidate certain basic genetic processes including mutation, gene expression and complementation. Sixty-nine galactose-negative clones were established after mutagenic treatment of cells with 5-bromodeoxyuridine and black light. In contrast to the parental cells, these mutants could not utilize exogenous galactose, mannose, fructose, galactose-l-phosphate, glucose-l-phosphase, or glucose-6-phosphate. Permeation of galactose into mutant cells appeared unimpaired. The pleiotropic nutritional response was due not to deficiency of any one specific enzyme in galactose catabolic pathway but to significant reduction in activities of many enzymes tested. We postulate that the mutant phenotype could be due to mutations at a regulatory gene locus, or at a yet unknown locus with enzymic defect that causes secondary metabolic imbalances. Following chemical mutagenic treatment of hamster cells, a number of variant clones have been isolated which may involve either the structural or regulatory gene loci in pyrimidine or amino acid metabolism. Biochemical and genetic characterizations of these isolates are in progress. BIBLIOGRAPHIC REFERENCE: Sun, N.C., C.C. Chang and E.H.Y. Chu. Mutant hamster cells exhibiting a pleiotropic effect on carbohydrate metabolism. Proc. Nat. Acad. Sci. U.S.A. 72: 469-473, 1975.